diphenylhydantoin/necrosis

A patient with post-traumatic seizure disorder developed lymphadenopathy, exfoliative dermatitis, and hepatic failure while on diphenylhydantoin therapy and died in hepatic coma. Autopsy disclosed massive hepatic necrosis. The clinical and pathological pictures are similar to the six previously

Isolated mouse islets exposed to 3mM glucose released an increased amount of insulin in the presence of acetazolamide (AZM) (10 mM) and diphenylhydantoin (DPH) (0.35 or 3.5 mM), whereas insulin secretion due to 20 mM glucose was decreased in the presence of AZM (10 mM) and DPH (0.35, 0.70 or 3.5

Sixty-three children with seizure disorders receiving phenobarbital and/or diphenylhydantoin for more than 12 months had liver function tests evaluated. All 56 whose serum anticonvulsant concentrations were in the therapeutic range had elevations of their serum gamma glutamyl transpeptidase

Although the toxicity of diphenylhydantoin in a number of target organs is discussed in numberous reports, hepatotoxic reactions are quite rare. The hepatic lesion has mostly been described as necrosis or hepatitis. Tissue sections from 20 patients who had validated diphenylhydantoin hepatotoxicity

We have developed a host-mediated assay system for detection of the transforming activity of chemical carcinogens on peritoneal macrophages, directly, as well as indirectly acting carcinogenic substances administered intraperitoneally to NMRI mice could be examined in this way. Resident macrophages

Pulmonary vascular inflammatory disorders may involve all components of the pulmonary vasculature, including capillaries. The principal histopathologic features of pulmonary capillaritis include capillary wall necrosis with infiltration by neutrophils, interstitial erythrocytes, and/or hemosiderin,